The accumulation of CO2 in the atmosphere and resulting ocean acidification represent a threat to marine ecosystems. While acid–base regulatory capacity is well developed in marine fish, allowing compensation of extra-cellular pH during short-term hypercapnia, the possible energetic costs of such regulation during long-term exposure remain to be established. In this study, juvenile European sea bass (Dicentrarchus labrax) were exposed from 2 days post-hatching to three different ocean acidification scenarios: control (present condition, PCO2 = 520 µatm, pH 7.9), moderate acidification (PCO2 = 950 µatm, pH 7.7), and high acidification (PCO2 = 1490 µatm, pH 7.5). After 1.5 years of exposure, fish aerobic metabolic capacities, as well as elements of their oxygen extraction and transport chain, were measured. Compared to control, PCO2 treatments did not affect fish standard metabolic rate (SMR). However, the most severe acidification condition was associated with a significantly elevated maximum metabolic rate (MMR).This was supported by heavier gill system and higher blood haemoglobin concentration. A reduction of maximum cardiac frequency (fHmax) during incremental warming of anaesthetized fish was also observed in both acidification scenarios. On the other hand, the critical oxygen level (O2crit), the minimum oxygen level required to sustain SMR, did not differ among groups. The increased MMR, associated with maintained SMR, suggests that acid–base compensatory processes, although not increasing maintenance costs, may affect components of bass homeostasis, resulting in new internal physico-chemical conditions. The possibility that these alterations influence metabolic pathways and physiological functions involved in fish aptitude to maximally transport oxygen is discussed.